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Publication : An oncogenic role for alternative NF-κB signaling in DLBCL revealed upon deregulated BCL6 expression.

First Author  Zhang B Year  2015
Journal  Cell Rep Volume  11
Issue  5 Pages  715-26
PubMed ID  25921526 Mgi Jnum  J:228367
Mgi Id  MGI:5706867 Doi  10.1016/j.celrep.2015.03.059
Citation  Zhang B, et al. (2015) An oncogenic role for alternative NF-kappaB signaling in DLBCL revealed upon deregulated BCL6 expression. Cell Rep 11(5):715-26
abstractText  Diffuse large B cell lymphoma (DLBCL) is a complex disease comprising diverse subtypes and genetic profiles. Possibly because of the prevalence of genetic alterations activating canonical NF-kappaB activity, a role for oncogenic lesions that activate the alternative NF-kappaB pathway in DLBCL has remained elusive. Here, we show that deletion/mutation of TRAF3, a negative regulator of the alternative NF-kappaB pathway, occurs in approximately 15% of DLBCLs and that it often coexists with BCL6 translocation, which prevents terminal B cell differentiation. Accordingly, in a mouse model constitutive activation of the alternative NF-kappaB pathway cooperates with BCL6 deregulation in DLBCL development. This work demonstrates a key oncogenic role for the alternative NF-kappaB pathway in DLBCL development.
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